Loading...
Regucalcin ameliorates doxorubicin-induced cytotoxicity in Cos-7 kidney cells and translocates from the nucleus to the mitochondria.
Mohammed, Noor A. Hakeem, Israa J. Hodges, Nikolas Michelangeli, Francesco
Mohammed, Noor A.
Hakeem, Israa J.
Hodges, Nikolas
Michelangeli, Francesco
Citations
Altmetric:
Advisors
Editors
Other Contributors
EPub Date
Publication Date
2022-01-01
Submitted Date
Collections
Files
Loading...
Article - VoR
Adobe PDF, 1.22 MB
Other Titles
Abstract
Doxorubicin (DOX) is a potent anticancer drug, which can have unwanted side-effects such as cardiac and kidney toxicity. A detailed investigation was undertaken of the acute cytotoxic mechanisms of DOX on kidney cells, using Cos-7 cells as kidney cell model. Cos-7 cells were exposed to DOX for a period of 24 h over a range of concentrations, and the LC50 was determined to be 7 µM. Further investigations showed that cell death was mainly via apoptosis involving Ca2+ and caspase 9, in addition to autophagy. Regucalcin (RGN), a cytoprotective protein found mainly in liver and kidney tissues, was overexpressed in Cos-7 cells and shown to protect against DOX-induced cell death. Subcellular localization studies in Cos-7 cells showed RGN to be strongly correlated with the nucleus. However, upon treatment with DOX for 4 h, which induced membrane blebbing in some cells, the localization appeared to be correlated more with the mitochondria in these cells. It is yet to be determined whether this translocation is part of the cytoprotective mechanism or a consequence of chemically induced cell stress.
Citation
Mohammed, N. A., Hakeem, I. J., Hodges, N., & Michelangeli, F. (2022). Regucalcin ameliorates doxorubicin-induced cytotoxicity in Cos-7 kidney cells and translocates from the nucleus to the mitochondria. Bioscience Reports, 42(1), BSR20211464. https://doi.org/10.1042/BSR20211464
Publisher
Portland Press
Journal
Bioscience Reports
Research Unit
PubMed ID
PubMed Central ID
Type
Article
Language
Description
Series/Report no.
ISSN
0144-8463
EISSN
1573-4935